中文摘要：

目的：研究细胞外信号调节蛋白激酶1／2（ERK1／2）通路在雄激素缺乏引起的勃起功能障碍（ED）中的作用。方法：8周龄健康雄性SD大鼠30只，随机分成对照组（A组）、去势组（B组）、去势后补充雄激素组（C组）。B组和C组大鼠均手术去势，其中C组大鼠在去势1周后注射十一酸睾酮（Tu）100mg/kg，其余组则注射等量生理盐水。1个月后测各组大鼠血清睾酮浓度、平均颈动脉压（MAP）、阴茎海绵体内压（ICP），通过Western印迹检测大鼠阴茎海绵体ERK1／2、内皮型一氧化氮合酶（eNOS）的蛋白表达。结果：B组大鼠血清睾酮[（1．27±0．48）nmol／L]较A组[（17．14±1．07）nmol／L]和C组[（16．24±1．90）nmol／L]明显降低（P〈0．05），ICP／MAP比值B组较A组和C组明显下降（P〈0．05）；Western印迹结果显示ERK1／2在各组中表达基本一致（P〉0．05），而磷酸化细胞外信号调节蛋白激酶1／2（P—ERK1／2）在B组中表达高于A组和C组（P〈0．05），eNOS在B组中表达明显低于A组和C组（P〈0．05）。结论：雄激素可能通过调控ERK1／2通路改善去势大鼠的勃起功能。

英文摘要：

Objective： To investigate the role of the extracellular signal-regulated protein kinase 1/2 （ERK1/2） pathway in erectile dysfunction （ED） caused by the absence of testosterone （T）. Methods： We randomly divided 30 eight-week-old healthy male SD rats into groups A （control）, B （castration）, and C （castration ＋ androgen replacement）. The rats in groups B and C were castrated surgically, and those in C injected with T undecanoate （ 100 mg/kg） at 1 week after castration, while the others with 0.9% normal saline instead. At 1 month after treatment, we determined the serum T level, intracavernous pressure （ICP）, and mean carotid arterial pressure （MAP） of the rats, and detected the expressions of ERK1/2 and endothelial nitric oxide synthase （eNOS） by Western blot. Results ： The serum T level was significantly lower in group B （ [ 1.27 ± 0.48 ] nmol/L） than in A （ [ 17.14 ±1.07 ] nmol/L） and C （ [ 16.24 ± 1.90 ] nmol/L） （ P 〈 0. 05 ）, and so were ICP and MAP （P 〈 0.05 ）. The expression of ERK1/2 showed no statistically significant differences among the three groups （P 〉 0.05 ）. , that of phosphatase ERK1/2 was markedly higher while that of eNOS remarkably lower in group B than in A and C （ both P 〈 0.05 ）. Conclusion ： Androgen replacement may improve the erectile function of castrated rats by regulating the ERK1/2 pathway.